A model of experimental autoimmune myocarditis (EAM), induced with cardiomyosin peptide specific T lymphocytes in female Lewis rats, was used to study acute hemodynamic and coronary vasculature changes. After injection of T cells 15 experimental animals (5 each at 1, 2 and 3 weeks) and 8 controls were studied using the isolated heart. The pO2 was measured using EPR oximetry. Effluent oxygen and coronary flow increased while coronary resistance decreased (p<.05) with EAM (1, 2 and 3 weeks). Heart/body weight increased while rate-pressure product, +dP/dt and -dP/dt decreased (p<.05) compared to controls at 1 week but not at 2 or 3 weeks. Myocardial oxygen consumption and mean pO2 were not different for EAM versus control. However, compared to controls EAM myocardial pO2 varied more widely and was often beyond the usual range, suggesting occurrence of localized hypoxic and hyperoxic areas. Decreased coronary resistance, increased coronary flow and pO2 heterogeneity are consistent with development of low resistance, high flow hyperoxic areas which steal flow causing hypoxia in other areas.